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通过TNF-α和细胞染色体c表达在牙髓中的LPS诱导的神经细胞亡

Galih Sampoerno¹, Eddo Supriyanto², Dian Agustin Wahjuningrum¹

¹Department of Conservative Dentistry, Faculty of Dental Medicine, Univeristas Airlangga, Surabaya, Indonesia.

European journal of dentistry

|December 4, 2023

概括

在牙髓中暴露的 Porphyromonas gingivalis 脂聚糖 (LPS) 可能会通过细胞外途径触发亡. 这一过程与瘤亡因子-α (TNF-α) 表达的增加有关,这表明细胞死亡的作用.

科学领域:

口腔生物学口腔生物学
免疫学免疫学免疫学
细胞病理学细胞病理学

背景情况:

牙纸中的细胞亡或编程细胞死亡可以由 Porphyromonas gingivalis. lipopolysaccharide (LPS) 等细菌成分诱导.
LPS激活类似收费受体 (TLRs),通过细胞内和细胞外机制启动炎症和亡反应.

研究的目的:

为了研究LPS暴露对牙纸内的神经元细胞的影响.
分析瘤亡因子-α (TNF-α) 和细胞染色体c (cyt-c) 的表达,以应对LPS.
阐明特定的途径 (细胞内与细胞外) 参与LPS诱导的牙纸的亡.

主要方法:

斯普拉格·道利大鼠的下牙被暴露在LPS中48小时.
对神经元细胞进行了组织病理学分析,使用血素-素染色.
间接免疫组织化学被用来评估TNF-α和cyt-c的表达.
逐步回归线性分析检查了神经元细胞,TNF-α和cyt-c之间的关系.

主要成果:

暴露于LPS导致牙纸中的神经元细胞数量减少.
在LPS暴露和TNF-α表达之间观察到显著的关系.
虽然与对照细胞相比,TNF-α表达在暴露于LPS的细胞中较高,但cyt-c表达与暴露于LPS没有显著的关系.
与对照组相比,TNF-α和cyt-c表达在LPS暴露后的神经元细胞中都增加了.

结论:

牙纸中的LPS暴露可以启动亡,可能是通过细胞外途径.
提升的TNF-α表达是牙纸中LPS诱导的亡的关键指标.
这些发现有助于了解脉炎和细菌诱导的细胞死亡的分子机制.

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